Human cytomegalovirus (CMV) infections are a substantial source of morbidity and mortality in transplant recipients, and a major cause of long-term disabilities in congenitally infected children. Because of this, the development of new antiviral therapies is urgently needed. The ability of this virus to undergo lifelong latency and reactivation cycles, however, represents a formidable obstacle in our progress towards this goal. Here, we propose to use two in vitro models of CMV latency in hematopoietic cells to conclusively establish if and how maintenance of latent viral genomes is achieved in dividing myeloid progenitor cells. This work will provide significant insights into a crucial aspect of CMV latency, and will constitute the foundation for the development of innovative therapies with the potential to eradicate this virus from the human population.